Acute lung injury (ALI) is a complex multi-factorial syndrome which manifests as leaky lung microvessels, protein-rich alveolar edema, and hypoxemia that is intractable to ventilation with high levels of oxygen. The patients are often septic, and at present, only different modes of ventilator therapy are used for their clinical management. Most therapeutic modalities, including extracorporeal oxygenation, corticosteroids, prostaglandins, surfactant, and nitric oxide, generally fail to improve outcome (Fulkerson, et al. (1996) Arch. Intern. Med. 156: 29-38). The pathophysiology of ALI remains unclear. However, a common finding is the recruitment and activation of inflammatory cells into the lung (Brennan, et al. (1995) Br. Med. Bull. 51: 368-384; Rahman & MacNee (1995) Thorax 51:348-350). Airway epithelial cells have also been shown to act as immune effectors by secreting proinflammatory mediators (Thompson, et al. (1995) Eur. Respir. 8: 127-149). Once triggered, the inflammatory response results in lung inflammation, neutrophils sequestration in lungs, and increased microvascular permeability leading to plasma leakage into lung tissue and excessive fluid accumulation in airspaces. Prognosis of these critically ill patients is typically poor with mortality ranging from 50% to 60% among the 150,000 to 180,000 patients diagnosed annually, which is more fatal than breast tumor and HIV/AIDS disease combined (Ware & Matthay (2005) NEJM 353: 2788-96). At present ventilator therapy is used for their clinical management. Unfortunately, there are no conventional therapies available to restore the integrity of the microvascular endothelial barrier (the key underlying factor in edema formation), thereby preventing the accumulation of protein-rich fluid in the extravascular space and promoting productive wound healing.